ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020
High-fat diet-induced GAIT element-mediated translational silencing of mRNAs encoding inflammatory proteins in macrophage protects against atherosclerosis.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Article
- Myeloid-specific deficiency of ribosomal protein L13a alters macrophage polarity and diversity during differentiation from bone marrow.Journal of leukocyte biology · 2025Article
- Ribosomal proteins: the missing piece in the inflammation puzzle?Molecular and cellular biochemistry · 2025Review
- Loss of function of ribosomal protein L13a blocks blastocyst formation and reveals a potential nuclear role in gene expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- A Structurally Conserved RNA Element within SARS-CoV-2 ORF1a RNA and S mRNA Regulates Translation in Response to Viral S Protein-Induced Signaling in Human Lung Cells.Journal of virology · 2022Article
- Targeting epigenetic modifiers to reprogramme macrophages in non-resolving inflammation-driven atherosclerosis.European heart journal open · 2021Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Previously, we identified a mechanism of inflammation control directed by ribosomal protein L13a and "GAIT" (Gamma Activated Inhibitor of Translation) elements in target mRNAs and showed that its elimination in myeloid cell-specific L13a knockout mice (L13a KO) increased atherosclerosis susceptibility and severity. Here, we investigated the mechanistic basis of this endogenous defense against atherosclerosis. We compared molecular and cellular aspects of atherosclerosis in high-fat diet (HFD)-fed L13a KO and intact (control) mice. HFD treatment of control mice induced release of L13a from 60S ribosome, formation of RNA-binding complex, and subsequent GAIT element-mediated translational silencing. Atherosclerotic plaques from HFD-treated KO mice showed increased infiltration of M1 type inflammatory macrophages. Macrophages from KO mice showed increased phagocytic activity and elevated expression of LDL receptor and pro-inflammatory mediators. NanoString analysis of the plaques from KO mice showed upregulation of a number of mRNAs encoding inflammatory proteins. Bioinformatics analysis suggests the presence of the potential GAIT elements in the 3'UTRs of several of these mRNAs. Macrophage induces L13a/GAIT-dependent translational silencing of inflammatory genes in response to HFD as an endogenous defense against atherosclerosis in ApoE
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